From the Department of Neurosurgery (M.M., N.A., C.M.P., E.T., N.P.), Department of Bioengineering (N.P.), Neuroscience Interdepartmental Program (N.P.), Brain Research Institute (N.P.); and Department of Anesthesiology (A.E.H.), University of California, Los Angeles, California.
Anesthesiology. 2018 Feb;128(2):305-316. doi: 10.1097/ALN.0000000000001940.
Anesthetics are believed to alter functional connectivity across brain regions. However, network-level analyses of anesthesia, particularly in humans, are sparse. The authors hypothesized that propofol-induced loss of consciousness results in functional disconnection of human sensorimotor cortices underlying the loss of volitional motor responses.
The authors recorded local field potentials from sensorimotor cortices in patients with Parkinson disease (N = 12) and essential tremor (N = 7) undergoing deep brain stimulation surgery, before and after propofol-induced loss of consciousness. Local spectral power and interregional connectivity (coherence and imaginary coherence) were evaluated separately across conditions for the two populations.
Propofol anesthesia caused power increases for frequencies between 2 and 100 Hz across the sensorimotor cortices and a shift of the dominant spectral peak in α and β frequencies toward lower frequencies (median ± SD peak frequency: 24.5 ± 2.6 Hz to 12.8 ± 2.3 Hz in Parkinson disease; 13.8 ± 2.1 Hz to 12.1 ± 1.0 Hz in essential tremor). Despite local increases in power, sensorimotor cortical coherence was suppressed with propofol in both cohorts, specifically in β frequencies (18 to 29 Hz) for Parkinson disease and α and β (10 to 48 Hz) in essential tremor.
The decrease in functional connectivity between sensory and motor cortices, despite an increase in local spectral power, suggests that propofol causes a functional disconnection of cortices with increases in autonomous activity within cortical regions. This pattern occurs across diseases evaluated, suggesting that these may be generalizable effects of propofol in patients with movement disorders and beyond. Sensorimotor network disruption may underlie anesthetic-induced loss of volitional control.
人们认为麻醉剂会改变大脑区域之间的功能连接。然而，麻醉的网络水平分析，特别是在人类中，仍然很少。作者假设异丙酚诱导的意识丧失导致与自主运动反应丧失相关的感觉运动皮质的功能分离。
作者记录了帕金森病（N=12）和原发性震颤（N=7）患者在接受深部脑刺激手术前和异丙酚诱导意识丧失后感觉运动皮质的局部场电位。在两种人群中，分别评估了条件之间的局部光谱功率和区域间连接（相干性和虚相干性）。
异丙酚麻醉导致感觉运动皮质的 2 到 100 Hz 之间的频率的功率增加，并且α和β频率的主导频谱峰值向较低频率转移（帕金森病的中位数±SD 峰值频率：24.5±2.6 Hz 到 12.8±2.3 Hz；原发性震颤：13.8±2.1 Hz 到 12.1±1.0 Hz）。尽管局部功率增加，但在两个队列中，异丙酚都抑制了感觉运动皮质的相干性，特别是在帕金森病的β频率（18 到 29 Hz）和原发性震颤的α和β频率（10 到 48 Hz）。
尽管局部光谱功率增加，但感觉和运动皮质之间的功能连接减少表明，异丙酚导致皮质区域自主活动增加的皮质功能分离。这种模式在评估的疾病中都存在，这表明这些可能是异丙酚在运动障碍患者和其他患者中普遍存在的作用。感觉运动网络中断可能是麻醉诱导的自主控制丧失的基础。
